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相关概念视频

DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
Abnormal Proliferation02:23

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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
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Updated: Jun 10, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

p53AIP1,是p53-依赖性亡的潜在媒介,并通过Ser-46-phosphorylated p53进行其调节.

K Oda1, H Arakawa, T Tanaka

  • 1Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, University of Tokyo, Japan.

Cell
|October 13, 2000
PubMed
概括
此摘要是机器生成的。

研究人员发现了p53AIP1,一种诱导亡的新型基因. 它的表达是通过p53酸化在Ser-46调节的,这对DNA损伤反应和细胞死亡至关重要.

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Yeast As a Chassis for Developing Functional Assays to Study Human P53
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科学领域:

  • 分子生物学分子生物学
  • 细胞生物学 细胞生物学
  • 遗传学 遗传学 是一个

背景情况:

  • 瘤抑制蛋白p53在细胞对DNA损伤的反应中起着至关重要的作用.
  • 通过p53介导的亡是消除受损细胞和预防癌症的关键机制.
  • 通过p53诱导亡的精确分子机制仍在被阐明.

研究的目的:

  • 确定参与亡的由p53调节的新型基因.
  • 研究一个新发现的基因p53AIP1在p53-依赖性亡中的作用.
  • 确定p53酸化在Ser-46在调节亡中的重要性.

主要方法:

  • 从人类基因组DNA中直接克隆p53结合序列.
  • 细胞中p53AIP1的宫外表达和其局部化和亡效应的评估.
  • 在对DNA损伤的反应中对Ser-46中的p53酸化的分析.
  • 局部定向突变发生,以替代p53的Ser-46并评估其对亡和p53AIP1表达的影响.

主要成果:

  • 一个新的基因,p53AIP1 (p53-调节的亡诱导蛋白1),被确定并被发现可以被野生类型的p53.3诱导.
  • 细胞外表达的p53AIP1将其定位到线粒体,并通过线粒体膜潜能 (A(psi) m) 的消散诱导细胞死亡.
  • 严重的DNA损伤诱导了p53在Ser-46的酸化,这对于诱导亡和选择性表达p53AIP1.1至关重要. 替代Ser-46取消了p53的亡功能和p53AIP1的表达.

结论:

  • p53AIP1是p53-依赖性亡的关键调解者.
  • 在Ser-46中对p53的酸化是一个关键的调节事件,它控制了诱导亡的基因p53AIP1.1的转录激活.
  • 这一发现为控制p53诱导的亡反应于DNA损伤的分子途径提供了新的见解.